Definition

Acute limb ischemia occurs when a leg or foot suffers from inadequate blood flow to maintain vital metabolic functions. Both arterial embolism and arterial (or bypass graft) thrombosis commonly precipitate acute limb ischemia.

Prevalence and Epidemiology

The incidence of acute limb ischemia is approximately 1.7/10,000 per year.³ Patients presenting with a pulseless extremity suffer amputation rates as high as 10% and mortality rates of 5% to 15%.^4,5 These patients are characteristically at high risk for perioperative complication and are medically fragile (Table 113-1).

Etiology and Pathophysiology

Limb ischemia can result acutely from a variety of causes (Table 113-2). Sudden-onset acute pain is indicative of an embolic event; a history of chronic pain or claudication before the acute ischemic episode is suggestive of a thrombotic etiology. Graft occlusions are slightly more common than thromboses of native arteries. Thrombotic occlusions are approximately six times more common than embolic events.

TABLE 113-2 Causes of Acute Limb Ischemia

Clinical Presentation

Patients commonly present within hours of the onset of pain. Lower extremity ischemia presents with six p’s—pain, pallor, paresthesias, paralysis, pulselessness, and poikilothermia. In general, limb ischemic symptoms and signs will be present at a level one joint below the acute occlusive phenomenon; for example, common femoral artery occlusion will result in foot and calf pain. Normal proximal and contralateral pulse examination findings are indicative of an embolic event in an otherwise normal vascular tree. In contrast, evidence of diffuse chronic atherosclerotic disease suggests a thrombotic etiology of the acute ischemia.

Muscle and nerve tissues are able to tolerate no more than 6 hours of profound ischemia. The patient will experience a variable sensory deficit. In extreme cases, the affected limb will be insensate to even penetration of a needle into the muscles of the foot or calf; use of a sterile 19-gauge needle may allow the clinician to objectively determine whether any sensation remains. Paralysis (motor deficit) is a poor prognostic sign indicating relatively profound ischemia. Deficits in dorsiflexion and plantar flexion of the foot, which are accomplished by the muscles of the leg, are indicative of more extensive ischemia and a more proximal occlusive arterial lesion than are weakness and paralysis of the intrinsic muscles of the foot.

Because of its acuity and thus the absence of adequate preformed collateral arteries, arterial embolization is the classic situation resulting in acute arterial occlusion and acute limb ischemia. The anatomic distribution of arterial embolism is depicted in Figure 113-1. The embolus most frequently lodges at an arterial bifurcation.

FIGURE 113-1 The most common sites of arterial embolic occlusions.

In the patient with bilateral lower extremity ischemia and absent femoral pulses, the most common clinical scenario is saddle embolus to the aortic bifurcation. The patient will complain of sudden onset of bilateral buttock and lower extremity pain. Mottling of the lower extremities and lower abdomen, sometimes up to the umbilicus, will be evident on physical examination. The diagnosis in these patients is too frequently missed, probably because of the bilateral nature of the ischemic insult. Even in the setting of absent femoral pulses, patients are often evaluated for possible neurologic or neurosurgical problems, resulting in a delay of diagnosis and appropriate therapy. This disease can carry with it a poor prognosis, with a 27% mortality in one modern series.⁷

The most common site of clinically significant embolism in the lower extremity is the common femoral artery bifurcation.⁸ Patients with common femoral artery embolism will experience foot and calf pain. Finally, an embolus to the popliteal artery will result in absent pedal pulses and an ischemic foot.

Approximately 90% of the time, arterial emboli arise in the heart.⁹ Atrial fibrillation results in a dilated, noncontractile left atrial appendage, which predisposes to thrombus formation and—on spontaneous or therapeutic cardioversion—thromboembolism. Left ventricular thrombus may also form, for instance, adjacent to a noncontractile left ventricular segment after myocardial infarction, in a left ventricular aneurysm, or in the setting of dilated cardiomyopathy. Saddle emboli, which lodge at the aortic bifurcation and cause bilateral lower extremity ischemia, are most commonly the result of left ventricular thrombus. Thromboembolism from heart valves are less common today than in the past owing to the relative decrease in prevalence of rheumatic heart disease. Bacterial endocarditis can result in septic emboli that may cause both acute ischemia and infection of the distal vessel wall, which in turn results in mycotic aneurysm. Atheroemboli may arise from either the thoracic or the abdominal aorta. Finally, in some 5% of cases, the source of embolism is never identified.

Clinical Categorization of Acute Limb Ischemia

Since 1997, the Rutherford criteria have been used to grade the clinical severity of acute limb ischemia.¹⁰ These grades, as summarized in Table 113-3, are indicative both of whether emergent surgical intervention is indicated and of whether the limb is salvageable. Most commonly, category I represents an acute occlusion in a chronically narrowed artery, with well-formed collaterals. Category II represents a limb that is salvageable with immediate therapy or intervention. In the case of irreversible ischemia, category III, the patient will present with profound vascular and neurologic deficits; the limb may be in a state of rigor mortis and will require amputation.

TABLE 113-3 Clinical Categorization of Acute Limb Ischemia

Before imaging studies, in patients with acute limb ischemia, laboratory studies are indicated. In particular, and in anticipation of imaging studies with use of nephrotoxic contrast agents, a serum creatinine concentration should be obtained. If a hypercoagulable state is suspected, a hypercoagulable profile should be sent before institution of any anticoagulation. An electrocardiogram will aid in the diagnosis of atrial fibrillation and will provide some information as to the patient’s cardiac status. Assessment of the patient’s cardiac risk for general anesthesia by the Goldman index or other scale may be useful.¹¹

Doppler examination of the lower extremity may be useful, with attention to both arterial and venous signals. When arterial signals are present in the ankle, at either the dorsalis pedis or the posterior tibial artery, the ankle-brachial index should be measured. The absence of venous “hums” indicates more severe ischemia.

In limbs ischemic for 4 to 6 hours, significant reperfusion injury and swelling may occur. Swelling may result in increased compartment pressures, typically presenting earliest in the anterior compartment of the leg, which has both a significant mass of slow-twitch red muscle fibers and a strong encasing fascial envelope. The contents of the anterior compartment include the deep peroneal nerve, the tibialis anterior muscle, and the anterior tibial artery; compartment syndrome with accompanying tissue necrosis in this distribution classically results in footdrop.

Whereas some surgeons will elect to observe a transiently ischemic limb for signs of compartment syndrome postoperatively, in the setting of more than 6 hours of profound ischemia, many perform four-compartment fasciotomies prophylactically at the time of revascularization. If one elects to observe the patient’s leg, any increased pain, especially with passive plantar flexion of the foot, or loss of sensation in the first web space of the foot (sensory distribution of the deep peroneal nerve) should prompt reevaluation. Compartment pressures may be measured by a Stryker needle (Stryker Instruments, Kalamazoo, MI) or other device. Compartment pressure of greater than 30 mm Hg can result in tissue ischemia and necrosis. Patients demonstrating hypotension or shock, those requiring pressors, those with absent flow through the popliteal artery at presentation, and younger patients with greater muscle mass and fewer arterial collaterals are at increased risk for development of compartment syndrome. Four-compartment fasciotomy is usually performed through both a medial and a lateral incision (Fig. 113-2). The incisions are left open for subsequent delayed primary closure or skin grafting.

FIGURE 113-2 Four-compartment fasciotomy of the leg is usually performed through both medial and lateral incisions, but it can be performed through a lateral incision only.

(From Velmahos GC, Toutouzas KG. Vascular trauma and compartment syndromes. Surg Clin North Am 2002; 88:1.)

Rhabdomyolysis can occur in patients whose limbs have suffered significant ischemia-reperfusion injury from arterial occlusion. This clinical entity should be suspected in patients with acute limb ischemia demonstrating increased muscle pain and weakness, renal failure, or hyperkalemia. Useful laboratory tests include urinalysis and serum creatine kinase concentration. The urine dip will be positive for blood, whereas the microscopic urinalysis will not demonstrate significant numbers of red blood cells; urinalysis will also demonstrate casts and myoglobin. Treatment consists of volume expansion (with goal urine output of 1 to 2 mL/kg/hr) and alkalinization of the urine with sodium bicarbonate infusion. If the patient does not succumb to the primary illness or acute renal failure, renal compromise in those patients suffering rhabdomyolysis generally resolves.

Imaging Indications and Algorithm

Arteriography is the gold standard for diagnosis and anatomic evaluation of acute limb ischemia. However, other imaging modalities at times merit consideration.

Imaging Techniques and Findings

Medical

Acute limb ischemia is a surgical disease; however, attention to the patient’s medical and overall condition is essential. Maintenance intravenous fluids should be initiated and the patient kept nil per os. A Foley catheter should be inserted to monitor urine output. Consideration should be given to either oral acetylcysteine¹⁴ or bicarbonate infusion¹⁵ if the patient has chronic renal insufficiency or diabetes because diagnostic or completion angiography will likely be indicated.

Temperature extremes and fluctuations should be avoided; cold temperatures cause vasoconstriction, and heat causes increased tissue metabolic demands. Transfusion and optimization of cardiac output should be accomplished whenever these might result in improved oxygenation of the affected limb.

Surgical/Interventional

Intra-arterial or catheter-directed thrombolysis or fibrinolysis has proved effective and beneficial in a variety of clinical scenarios involving acute limb ischemia.^16–18 However, in a number of situations, thrombolytics are absolutely contraindicated; these include recent surgery or trauma, recent stroke, active bleeding diathesis, and recent history of gastrointestinal bleeding. In some cases, percutaneous aspiration or mechanical thrombectomy is used before and in conjunction with thrombolysis. It is essential that any stenoses revealed on arteriography after thrombolysis be treated with angioplasty, bypass graft revision, or revascularization. In the interim from completion of thrombolysis until intervention directed at flow-limiting lesions, heparin infusion must be continued.

Before 1963 and the introduction of Thomas J. Fogarty’s balloon embolectomy catheter (Fig. 113-3), only 23% of patients suffering embolic vascular occlusion were treated surgically with embolectomy. Subsequent to the introduction of this catheter and continuing today, most of these patients undergo surgical embolectomy, which now—along with systemic anticoagulation—is the mainstay of therapy.

FIGURE 113-3 Original patent application for Fogarty embolectomy catheter.

(From archives of U.S. Patent and Trademark Office, with permission.)

Aortic occlusion may result from aortic saddle embolus, in situ thrombosis of an atherosclerotic abdominal aorta, thrombosis of an abdominal aortic aneurysm, or aortic dissection. It is important to establish the etiology of aortic occlusion because balloon catheter embolectomy through a femoral cutdown (see later) is usually successful in the setting of saddle embolus but is infrequently helpful in patients with in situ thrombosis of a chronically diseased abdominal aorta. In the latter scenario, the limbs are usually not profoundly ischemic owing to the chronic nature of the disease and resulting extensive collateralization; these patients may require aortobifemoral grafting to reestablish lower extremity perfusion.

Acute unilateral iliac occlusion can occur in patients having undergone prior aortic aneurysmorrhaphy with a bifurcated graft, prior aortobifemoral reconstruction, or prior abdominal aortic stent grafting. In these situations, the surgeon may be able to restore patency of the graft limb with balloon thrombectomy performed from a groin incision, but a technical problem in the affected limb and graft stenosis must be suspected and subsequently addressed (Fig. 113-4).¹⁹ If limb patency cannot be reestablished, femoral-femoral or axillofemoral bypass is indicated.

FIGURE 113-4 A, Occluded left limb of an abdominal aortic stent graft. Wire access to the aorta was accomplished from the patient’s groin bilaterally. Stents were placed in the newly patent left iliac limb to displace residual thrombus and to treat any stenoses that might have contributed to the thrombosis. B, Completion angiogram.

Symptomatic popliteal aneurysms generally present with limb ischemia—from aneurysm thrombosis or distal thromboembolism—rather than with rupture. The diagnosis should be suspected in any patient with acute or chronic ischemia of the leg and a palpable firm pulseless (in the case of thrombosis) or pulsatile mass behind the knee. Duplex ultrasound examination can confirm the diagnosis. Angiography, MRA, and CTA are useful for operative planning. Treatment of a popliteal aneurysm presenting with acute limb ischemia consists of emergent catheter-directed thrombolysis to reestablish distal arterial patency²⁰ and subsequent surgical exclusion and bypass; resection of the aneurysm is not necessary. There is also an emerging experience with covered stents for treatment of popliteal aneurysms.²¹ Half of patients will have bilateral popliteal aneurysms, and one third of patients with a popliteal aneurysm will have a coincident abdominal aortic aneurysm; therefore, these patients should be screened for coexisting aneurysmal disease.

In patients suffering from thrombotic arterial occlusions and in those whose thromboembolism cannot be extracted or lysed, arterial bypass grafting may be necessary to treat stenotic or occluded vascular segments. Surgical arterial bypass and other revascularization procedures are detailed in Chapter 114.

Definition

Atherosclerosis resulting in peripheral arterial disease is the most common cause of chronic limb ischemia. Chronic limb ischemia presents as a spectrum of disease from asymptomatic to claudication to critical limb ischemia. This spectrum is encapsulated in two similar staging systems for peripheral arterial disease: Fontaine stages and Rutherford categories (Table 113-4).

Symptomatic patients with peripheral arterial disease generally present with either intermittent claudication or critical limb ischemia. Intermittent claudication is defined as muscle discomfort in the lower limb reproducibly produced by exercise and relieved by rest within 10 minutes. Critical limb ischemia is defined as persistent, recurring ischemic rest pain requiring opiate analgesia for at least 2 weeks with ulceration or gangrene of the foot or toes. Hence, Rutherford categories 4 through 6 comprise those patients with critical limb ischemia.¹

Of course, there is significant overlap between critical limb ischemia and acute limb ischemia. However, the rational construct differentiating patients with immediately threatened limbs and those with chronically threatened legs is clinically useful.

Prevalence and Epidemiology

Intermittent claudication has a prevalence of approximately 3% in 40-year-olds and about 6% in 60-year-olds. Claudication often is not progressive; revascularization is required in less than one quarter of patients at 10 years, and amputation is required in approximately 2% of patients at 5 years. However, continued smoking or coexistent diabetes portends worse clinical outcomes for claudicants, including more frequent eventual amputation. The outcome of intermittent claudication at 5 years is summarized in Figure 113-5.

FIGURE 113-5 Fate of the claudicant during 5 years. CLI, critical limb ischemia; CV, cardiovascular; MI, myocardial infarction; PAD, peripheral arterial disease.

(From Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease. J Am Coll Cardiol 2006; 47:1239-1312.)

Critical limb ischemia has an incidence in the United States of approximately 1000 new cases per 1 million population. Figure 113-6 summarizes risk factors for the development of critical limb ischemia in patients with peripheral arterial disease. More than half of patients with critical limb ischemia undergo attempts at revascularization as definitive treatment; regardless, significant numbers of patients lose their limbs or die within 1 year (Fig. 113-7).

FIGURE 113-6 Approximate magnitude of the effect of risk factors on the development of critical limb ischemia in patients with peripheral arterial disease. ABPI, ankle-brachial pressure index; CLI, critical limb ischemia.

(From Norgren L, Hiatt WR, Dormandy JA, et al; TASC II Working Group. Inter-Society Consensus for the Management of Peripheral Arterial Disease [TASC II]. J Vasc Surg 2007; 45[Suppl S]:S5-S67.)

FIGURE 113-7 Fate of patients presenting with critical leg ischemia (CLI).

(From Norgren L, Hiatt WR, Dormandy JA, et al; TASC II Working Group. Inter-Society Consensus for the Management of Peripheral Arterial Disease [TASC II]. J Vasc Surg 2007; 45[Suppl S]:S5-S67.)

Risk factors for peripheral arterial disease include smoking, diabetes, hypertension, chronic renal insufficiency, African-American race, male sex, hyperlipidemia, and hyperhomocysteinemia.

Again, the importance of chronic limb ischemia as a marker for atherosclerotic cardiovascular disease cannot be overstated. The 5-year mortality rate is 30% for patients with claudication and 70% for patients with critical limb ischemia.

Etiology and Pathophysiology

Peripheral arterial disease most commonly results from atherosclerosis of the distal arterial tree (i.e., aortic bifurcation and below) and is manifested typically as intermittent claudication. Patients with intermittent claudication have normal blood flow to the limb at rest; but with exercise, the occlusive arterial disease prevents proper augmentation of blood flow, resulting in insufficient oxygen delivery to the muscles and the symptoms of claudication. Critical limb ischemia represents more advanced occlusive peripheral arterial disease in which oxygen delivery to the lower limb is suboptimal even at rest.

Manifestations of Disease

Clinical Presentation

Intermittent Claudication

Patients with intermittent claudication describe fatigue, aching, or cramping in the muscles of the leg that develops after walking a consistent established distance (or other exercise) and that resolves with rest. These symptoms most often appear in the calf but can affect the thigh or buttocks. The anatomic site of pain frequently corresponds to the level of occlusive disease; symptoms typically present in muscle groups one joint level below the region of arterial occlusion. Thus, calf muscle claudication is most commonly due to superficial femoral artery occlusion; hip, thigh, or buttock claudication is most commonly due to more proximal aortoiliac disease.

A complete physical examination should focus on cardiovascular diseases. The blood pressure should be measured in both arms and the ankle-brachial index in each leg. Auscultation is performed to assess for cardiac disease. The abdomen is palpated in an attempt to detect an abdominal aortic aneurysm as a potential embolic source (although physical examination is only 50% sensitive for abdominal aortic aneurysms 4 to 5 cm in diameter).

The peripheral vascular examination comprises palpation of the radial, ulnar, brachial, carotid, femoral, popliteal, dorsalis pedis, and posterior tibial pulses. Especially prominent femoral or popliteal pulses should suggest aneurysm disease. Auscultation of the carotid, abdominal aorta, and iliac arteries and femoral artery can suggest occlusive vascular disease. In addition, the skin of the legs should be assessed for skin color, temperature, or decreased hair growth and the muscles of the leg for ischemic atrophy.

Normal leg pulses do not rule out intermittent claudication as the diagnosis of a patient’s complaints; for instance, isolated internal iliac occlusive disease may cause buttock claudication (and impotence in men). In addition, in claudicants, pulses may be palpable at rest but absent with exercise; ankle-brachial indices can be performed before and immediately after exercise (usually on a treadmill) to document the claudication.

As suggested before, ankle-brachial indices constitute a first diagnostic test in patients thought to have intermittent claudication. First, the systolic blood pressure is measured in each arm, and the higher is taken as the brachial pressure. The cuff is then placed on the calf, inflated, and then slowly deflated; the highest pressure at which the Doppler signal—at either the posterior tibial or dorsalis pedis—becomes audible again marks the ankle pressure. A ratio of 1.0 is normal; an ankle-brachial index of less than 0.9 is clearly abnormal.

Critical Limb Ischemia

Patients with critical limb ischemia present with some combination of ischemic rest pain, nonhealing ulcers, and gangrene. Ischemic rest pain is severe, is intolerable, sometimes improves with lowering of the affected limb (dangling the foot over the edge of the bed), and is responsive only to narcotic analgesics. The pain is often worst at night (when the limb is elevated), sometimes wakes the patient from sleep, and is sometimes transiently relieved by rubbing the foot.

Except in cases of diabetic neuropathy and resulting anesthesia of the foot, patients with tissue loss of the lower extremity also often present with pain, localized to the wound. Ulcers and gangrene usually affect the toes, the heel and ankle, and, in severe cases, the distal foot proper. Ulcers are often initiated by minor trauma (e.g., ill-fitting shoes) or other injury (e.g., burn injury from attempts at warming a chronically painful cold foot).

In those patients with critical limb ischemia and diabetes mellitus, the peripheral neuropathy often contributes to the trauma initiating ulcer formation and to the delayed recognition of the wound by the patient. The microvascular derangement of diabetes predisposes to nonhealing of these wounds and to the subsequent development of infection (wet gangrene). Complications of diabetic foot ulcers, including gangrene, are the most common cause of nontraumatic leg, foot, and toe amputation. Up to 15% of diabetic patients will suffer from a foot ulcer during their lives, and 15% to 25% of these will require an amputation at some level.

The location and appearance of the ulcer or gangrene can provide the astute clinician a suggestion as to the etiology of the wound. For example, as indicated in Figure 113-8, calf ulcers are more often reflective of venous disease than of peripheral arterial disease.

FIGURE 113-8 The causes and frequencies of lower limb ulcers.

(From Norgren L, Hiatt WR, Dormandy JA, et al; TASC II Working Group. Inter-Society Consensus for the Management of Peripheral Arterial Disease [TASC II]. J Vasc Surg 2007; 45[Suppl S]:S5-S67.)

The putative diagnosis of critical limb ischemia should be confirmed by measuring ankle-brachial indices. Symptoms of rest pain commonly occur in patients with ankle pressures below 50 mm Hg. Peripheral arterial disease often impairs healing in leg ulcers caused by trauma, venous insufficiency, or neuropathy, and augmented blood flow (above that which would cause rest pain) is required to heal wounds or infections; therefore, ankle pressures below 70 mm Hg are suggestive of critical limb ischemia in patients with ulcers or gangrene.

Subsequently, pulse volume recordings may be performed by use of a plethysmograph in a vascular laboratory. This device measures volume changes in the limb at various levels with multiple blood pressure cuffs. Pulse volume recordings can localize arterial occlusive disease with up to 85% accuracy compared with angiography. Figure 113-9 demonstrates pulse volume recordings in a patient with unilateral superficial femoral artery occlusion before and after angioplasty and stenting of the superficial femoral artery.

FIGURE 113-9 Pulse volume recordings in a patient with superficial femoral artery occlusion, before (left) and after (right) recanalization, angioplasty, and stenting.

Differential Diagnosis

The causes of chronic leg ischemia apart from atherosclerosis include arteritis, popliteal artery entrapment, mucinous cystic degeneration, Buerger disease (thromboangiitis obliterans), Takayasu disease, aortic coarctation, popliteal aneurysm (with secondary thromboembolism), other embolic disease, fibromuscular dysplasia, pseudoxanthoma elasticum, thrombosis of persistent sciatic artery, endofibrosis of the external iliac artery (iliac artery syndrome in cyclists), and primary arterial tumors.

The differential diagnosis of intermittent claudication includes venous insufficiency, nerve root compression (sciatica or lumbar radiculopathy), symptomatic Baker cyst, chronic compartment syndrome (usually in heavily muscled athletes), spinal stenosis, hip arthritis, ankle arthritis, and foot arthritis.

In the case of critical limb ischemia with tissue loss, other causes of or factors contributing to the ulcer or gangrene must be considered. These include diabetes, venous insufficiency, neuropathies, musculoskeletal abnormalities causing disturbance in gait or mobility, infection, conventional trauma, calciphylaxis, and debility of any cause contributing to pressure or decubitus ulceration.²³

Synopsis of Treatment Options

Surgical/Interventional

In the case of severe intermittent claudication that has an impact on a patient’s livelihood or ability to perform activities of daily living, revascularization is sometimes indicated. Recent advances in and widespread adoption of endovascular therapy for peripheral arterial disease have lowered the threshold—in some practices—for attempted revascularization in patients with intermittent claudication. Meanwhile, revascularization is indicated and necessary in those patients with critical limb ischemia. Specific approaches and techniques for revascularization are discussed in Chapter 114.

Infection of the gangrenous toes, heel, foot, or leg in diabetic patients and in those with critical limb ischemia is often polymicrobial and present anywhere in the spectrum of local superinfection of preexisting ulcers to gas gangrene or necrotizing fasciitis of the leg. Principles of care include the initiation of broad-spectrum intravenous antibiotics until the organisms and their sensitivities are defined and the coverage can be narrowed. Débridement of infectious and gangrenous or necrotic tissue is essential. Amputation is seldom required but must be considered in certain cases. Revascularization is undertaken when the infection is under control.

Frequently, toe or forefoot amputations are undertaken to eliminate necrotic or infected tissue. When they are combined with temporally proximal revascularization, these amputations are classified as salvage procedures, allowing limb salvage in patients with ischemic gangrene of the foot. Not uncommonly in diabetic patients, toe amputation will be undertaken in the setting of unrevascularizable peripheral arterial disease or minimal peripheral arterial disease; diabetic neuropathy and vasculopathy are the causes of these gangrenous toes, and revascularization is not indicated.

Major amputation (below the knee or above the knee) is indicated when overwhelming infection threatens the patient’s life, when rest pain cannot be controlled or alleviated, or in the setting of a necrotic or gangrenous “dead” foot.

KEY POINTS

Peripheral arterial disease is the most common etiology of both chronic limb ischemia and acute limb ischemia.

Acute limb ischemia is a surgical emergency and is most often due to thromboembolus or acute thrombotic occlusion of a native artery or bypass graft.

Chronic limb ischemia can be manifested as either intermittent claudication or critical limb ischemia.

The mainstay of treatment for intermittent claudication is exercise therapy.

Revascularization is typically indicated in cases of critical limb ischemia that present with either rest pain or lower extremity ulcers or gangrene.